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Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
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Nitric oxide synthase inhibitors decrease coronary sinus-free radical concentration and ameliorate myocardial

Y Zhang1, J W Bissing, L Xu

  • 1Cardiovascular Center, University of Iowa, Iowa City, USA.

Journal of the American College of Cardiology
|August 14, 2001
PubMed
Summary

Inhibiting nitric oxide synthase with L-NNA reduced free radical generation and improved heart function after ischemia-reperfusion injury in dogs. This suggests a cardioprotective effect of blocking nitric oxide production during reperfusion.

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Area of Science:

  • Cardiovascular Research
  • Free Radical Biology
  • Ischemia-Reperfusion Injury

Background:

  • Ischemia-reperfusion sequences generate cardiotoxic free radicals.
  • Nitric oxide (NO) can react with superoxide to form peroxynitrite, increasing free radical formation.
  • Inhibiting NO production may offer cardioprotection by reducing oxidative stress.

Purpose of the Study:

  • To investigate the impact of NG-nitro-L-arginine (L-NNA), a nitric oxide synthase inhibitor, on free radical generation.
  • To assess the effect of L-NNA on myocardial contractility following ischemia-reperfusion.
  • To determine if inhibiting NO production is cardioprotective in an ischemia-reperfusion model.

Main Methods:

  • Studied 32 dogs undergoing 20-minute coronary occlusion-reperfusion.
  • Measured coronary sinus ascorbate free radical (Asc*-) concentration using electron paramagnetic resonance.
  • Administered L-NNA intravenously during occlusion-reperfusion; control dogs received saline. Assessed myocardial nitrotyrosine presence via immunohistochemistry.

Main Results:

  • L-NNA significantly reduced the rise in Asc*- concentration during reperfusion compared to controls (25% vs. 50% increase).
  • L-NNA preserved left ventricular fractional area shortening (FAS) during reperfusion (no significant change from baseline), unlike controls (significant decline).
  • Nitrotyrosine, a marker of peroxynitrite formation, was markedly reduced in L-NNA treated dogs.

Conclusions:

  • Inhibition of nitric oxide synthase with L-NNA decreases coronary sinus free radical levels.
  • L-NNA treatment ameliorates myocardial stunning following ischemia-reperfusion.
  • These findings support the hypothesis that reducing NO production can be cardioprotective against ischemia-reperfusion injury.